Prevalence of obesity in the United States
The prevalence of obesity in the United States is raising and will continue to rise. This increase is due to two major factors, lack of proper nutrition and sedentary jobs. There is a raising research evidence for an association between obesity and atherosclerotic cardiovascular disease (ASCVD) (Grundy, 2004). The cumulative risk factor that predisposes to ASCVD is known as metabolic syndrome. Obesity is a causal risk factor for (ASCVD), because as it increases the risk for ASCVD from other risk factors. The association of obesity to other significant and rising risk factors differs, depending individual’s acquire characteristics and genetic make-up(Grundy, 2002). Most of the people who are obese that develop ASCVD usually have a clustering of major risk factors (metabolic syndrome) known as metabolic risk factors (Grundy, 2004).
The biological basis of energy homeostasis
Energy homeostasis is a genetically multifaceted phenotype, whose molecular basis relies on passages connecting thousands of molecules. A better understanding on the regulation of genetic basis would provide the opportunity to create treatments for obesity and diabetes (Raab, 2006). The most important about energy homeostasis is the perception that alteration in energy stored in the body in the form of fat are conveyed to the central nervous system through negative feedback signals. This signals distribute in proportion to new changes in energy balance and to the content of body fat and, in the mist of different proposed regulatory food in-take signals, leptin and insulin became known as the best candidates to serve the adiposity signaling role( Schwartz and Niswender, 2004).
Nutrition, Obesity, and Atherosclerotic Cardiovascular Disease
Nutritional imbalances is a main cause to cell injury. Protein-calorie deficit can cause an awful number of deaths, mainly among disadvantaged populations. In addition, nutritional excesses is another important cause of cell injury. Thus, excesses of lipids influence to atherosclerosis, and obesity is a warning sign of the overloading of some cells in the body with fats (Warne, 2003). Atherosclerosis and obesity are prevalent in the United States. In addition to the problems of under-nutrition and over-nutrition, diet makes a significant differences (Warne, 2003). Atherosclerosis is a chronic inflammation response in the large and medium sized walls of arteries. Which is differentiated by the accumulation of macrophage white blood cell in vessel wall of cholesterol , and elevated by low density lipoproteins without sufficient removal of fats and cholesterol from the macrophages by functional high density lipoproteins(HDL). Diet is the main factor for atherosclerosis and hypertension, a major cardiovascular diseases affecting the developed world. This can be approached, in part, from a nutritional point of view. Diet is a multi-component mixture of several nutrients that can interrelate with one another (Getz, & Reardon, 2007).
Obesity has become a global epidemic, which is affecting children and adults of all ethnic groups, and is connected with considerable morbidity and mortality(Crowley, 2008). It is a disorder with a multifactorial etiology. Leptin, is a major player in energy homeostasis, which is the result of OB gene. The function OB gene anti-obesity factor was strengthened by the study that mice homozygous for mutations (OB/OB) gene lacks the ability to secrete leptin gene, tend to be severally obese, and with administration of exogenous leptin, this obese mice were cured. Blood leptin levels in obese individual are elevated because they cannot trigger the catabolic pathways. The reason for leptin resistance is not clear however it could be attributed to by the decline in the ability of leptin to cross over to the blood-brain wall, this is probably due to faulty transport across the endothelial cells. Thus, Obesity raises the risk of ischemic stroke in men and women, and abdominal obesity is linked with increased risk of venous thrombosis (Klein , Wadden , & Sugerman, 2002)
Recent and current research on Nutrition, Obesity, and Atherosclerotic Cardiovascular Disease
Obesity is the main risk factor for heart disease. it is imperative for physicians to be aware of rising research of novel approach in which adiposity negatively impact the heart as obesity continue to rise. Conventional wisdom suggests that either hemodynamic or metabolic disorder is linked with obesity that could be influences coronary artery disease and heart failure. Recent studies in healthy persons with heart failure exhibited that myocardial lipid content rises with the degree of adiposity and could attribute to the adverse structural and functional cardiac adaptations, which is seen in obese persons. These findings are similar with the observations found in the studies of obese animals and present support that myocardial lipid content could be a biomarker and accepted therapeutic target for cardiac disease in obese individuals (McGavock et al, 2006).
Currently an important and controversial concern is that atherogenes is the contribution as a result to diets. “The central question is, can dietary modification prevent or retard the development of atherosclerosis (most importantly, coronary artery disease)?” ( Bucher HC et al, 2002). In the United States the average individual consumes an excessive daily total of cholesterol and fat, with a proportion of about 3: 1of saturated fatty acids to polyunsaturated fatty acids. Some good source of cholesterol lowering lipid includes vegetable oils and fish oils that have polyunsaturated fatty acids. Fish oil that belong to the omega-3, group have more double bonds than omega-6, in vegetable oils. A current meta-analysis studies with over 15,000 people found that a diet rich in omega-3 fatty acids considerably lower the occurrence of lethal myocardial infarction and unexpected cardiac death ( Bucher HC et al, 2002).
Further, substantial evidence buttress the relationship between insulin resistance and vascular disease , which has led to broad “acceptance of the clustering of hyperlipidemia, glucose intolerance, hypertension, and obesity as a clinical entity, the metabolic syndrome” (Semenkovich, 2006). While for insulin resistance promoting the dyslipidemia and other metabolic irregularities, is part of the proatherogenic setting, which is likely that resistance from insulin in itself from the vascular wall cannot support atherosclerosis. Some Recent research advocates that insulin resistance and atherosclerosis might represent independent and eventually maladaptive reaction to the interruption of cellular homeostasis caused by the surplus delivery of energy (Semenkovich, 2006).
Public health’s application
Public health made recommendation on a nutritionally balanced diet, which is designed to reduce energy intake to be combined with other supportive interventions to accomplish a healthy body weight in overweight and obese persons of all ages (Lau et al, 2007) and to ensure the maintenance of energy homeostasis. The occurrence of obesity has raised from 23% to 31% in the United States, and 66% of adults are overweight (Christakis, & Fowler, 2007). A “clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults” was designed to target adults (age 18 years of age or older) who are at risk of developing metabolic syndrome and associated morbidities with a BMI of ≥25. Those with a BMI of 25 to 29.9 are regarded as overweight, and obese with BMI ≥30. Treatment is recommended for obesity when individuals exhibits two or more risk factors ( retrieved from American Journal of Clinical Nutrition)
Subsequently, there is a raising research evidence for an association between obesity and atherosclerosis. Some recent research exhibited that explicit-tissue knockout mice revealed an unexpected phenotypes, which suggests the existence of currently unknown crosstalk among organs and tissues ( Katagiri et al, 2007). In addition unraveling the complications of this inter-organ communication would improve the public health understanding of the development of obesity-associated diseases ( Katagiri et al, 2007)
Metabolism is not an independent procedure, isolated in the midst of different organs and tissues, but rather is synchronized and regulated throughout the body. To maintain the homeostasis of systemic metabolism, especially glucose and energy metabolism, metabolic coordinated regulation among organs and tissues is necessary ( Katagiri et al, 2007). Thus, any disruption of the metabolic coordinated control system could lead to the development of metabolic diseases.
Numbers of recent studies pointed out the occurrence of the metabolic syndrome is related with increased risk for both atherosclerotic cardiovascular disease (ASCVD) and type 2 diabetes. Individuals with the metabolic syndrome have about twice the increase in risk for ASCVD, compared with individuals without (Grundy, 2004). Though, the relationship between metabolic risk factors and development of ASCVD is multifaceted and clearly understood (Grundy, 2004).
The prevalence of obesity in the United States is rising and corresponds with the occurrence of metabolic syndrome and it is a cause for concern. Some recent study revealed that about 20 percent to 25percent of the US adult has metabolic risk factor. In some older groups, this occurrence is up to 50 percent (Grundy, 2002). Any efforts of the public health to prevent obesity in the context of the population should be a nationwide priority. From a clinical point of view, attention should focus on patients who are risk of developing the metabolic syndrome. Public health has made tremendous efforts in encouraging the public on the importance of properly diet, increased physical activity and weight loss in order to eliminate risk factors associated with obesity, and ASCVD (Grundy, 2002).
In conclusion, obesity should be acknowledged “as a product of free society in which a multitude of food choices and job opportunities are available” (Grundy, 2004). As a result any public health approach to the solve the obesity crisis that limits people’s choice would not be acceptable to the general public. Thus, this fact puts increased accountability on individuals to identify the underlying causes of obesity and alter their behavior to reduce the personal burden of obesity (Grundy, 2004)
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